Bystander suppression of experimental arthritis by nasal administration of a heat shock protein peptide

2011 ◽  
Vol 70 (12) ◽  
pp. 2199-2206 ◽  
Author(s):  
E. Zonneveld-Huijssoon ◽  
S. T. A. Roord ◽  
W. de Jager ◽  
M. Klein ◽  
S. Albani ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Experimental Arthritis ◽  
Nasal Administration ◽  
Bystander Suppression

Nasal administration of arthritis-related T cell epitopes of heat shock protein 60 as a promising way for immunotherapy in chronic arthritis

Biotherapy ◽  
1998 ◽  
Vol 10 (3) ◽  
pp. 205-211 ◽  
Author(s):  
Berent Prakken ◽  
Marca Wauben ◽  
Peter van Kooten ◽  
Steve Anderton ◽  
Ruurd van der Zee ◽  
...  
Keyword(s):  
T Cell ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Chronic Arthritis ◽  
Nasal Administration ◽  
Heat Shock Protein 60 ◽  
T Cell Epitopes

Self heat shock protein (Hsp) reactive T cells as regulatory cells in experimental arthritis

1997 ◽  
Vol 56 ◽  
pp. 379
Author(s):  
A.G.A. Paul ◽  
R. van der Zee ◽  
L.S. Taams ◽  
A. Bloemendal ◽  
P.J.S. van Kooten ◽  
...  
Keyword(s):  
T Cells ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Experimental Arthritis ◽  
Regulatory Cells

A Mycobacterial 65 kD Heat-Shock Protein and T Cells in Experimental Arthritis

2020 ◽  
pp. 253-268
Author(s):  
Willem van Eden ◽  
Claire J. P. Boog ◽  
Els J. M. Hogervorst ◽  
Marca H. M. Wauben ◽  
Ruurd van der Zee ◽  
...  
Keyword(s):  
T Cells ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Experimental Arthritis

scholarly journals Activation of T cells recognizing self 60-kD heat shock protein can protect against experimental arthritis.

1995 ◽  
Vol 181 (3) ◽  
pp. 943-952 ◽  
Author(s):  
S M Anderton ◽  
R van der Zee ◽  
B Prakken ◽  
A Noordzij ◽  
W van Eden
Keyword(s):  
T Cells ◽  
T Cell ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Amino Acid Identity ◽  
Cross Reactivity ◽  
Experimental Arthritis ◽  
Cell Recognition ◽  
T Cell Recognition ◽  
Normal Individuals

Lewis rats are susceptible to several forms of experimental arthritis-induced using heat-killed Mycobacterium tuberculosis (adjuvant arthritis, or AA), streptococcal cell walls, collagen type II, and the lipoidal amine CP20961. Prior immunization with the mycobacterial 65-kD heat shock protein (hsp65) was reported to protect against AA, and other athritis models not using M. tuberculosis, via a T cell-mediated mechanism. Hsp65 shares 48% amino acid identity with mammalian hsp60, which is expressed at elevated levels in inflamed synovia. Several studies have reported cross-reactive T cell recognition of mycobacterial hsp65 and self hsp60 in arthritic and normal individuals. We previously described nine major histocompatibility complex class II-restricted epitopes in mycobacterial hsp65 recognized by Lewis rat T cells. Of these only one, covering the 256-270 sequence, primed for cross-reactive T cell responses to the corresponding region of rat hsp60. Here we have tested each hsp65 epitope for protective activity by immunizing rats with synthetic peptides. A peptide containing the 256-270 epitope, which induced cross-reactive T cells, was the only one able to confer protection against AA. Similarly, administration of a T cell line specific for this epitope protected against AA. Preimmunization with the 256-270 epitope induced T cells that responded to heat-shocked syngeneic antigen-presenting cells, and also protected against CP20961-induced arthritis, indicating that activation of T cells, recognizing an epitope in self hsp60 can protect against arthritis induced without mycobacteria. Therefore, in contrast to the accepted concept that cross-reactive T cell recognition of foreign and self antigens might induce aggressive autoimmune disease, we propose that cross-reactivity between bacterial and self hsp60 might also be used to maintain a protective self-reactive T cell population. This discovery might have important implications for understanding T cell-mediated regulation of inflammation.

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